Stasis Dermatitis

Authors:
Alexander K. C. Leung, MD
Alberta Children’s Hospital, University of Calgary, Calgary, Alberta, Canada

Benjamin Barankin, MD
Toronto Dermatology Centre, Toronto, Ontario, Canada

Citation:
Leung AKC, Barankin B. Stasis dermatitis. Consultant. 2017;57(7):439-440.

A 77-year-old man presented with swelling of his ankles and the distal third of his legs, which had begun approximately 3 years ago. With time, the swelling had spread upward to involve the lower half of the legs. At the same time, the areas had become mildly pruritic and discolored, and the overlying skin had become thickened and waxy. He had had thrombophlebitis and deep vein thrombosis (DVT) of his legs approximately 5 years ago. His health was otherwise unremarkable, and he was not on any medications.

Physical examination revealed mottled, erythematous, edematous ankles and lower half of the legs. The overlying skin was thickened and indurated with an uneven texture and appearance. There was absence of body hair in the affected area. The rest of the physical examination findings were unremarkable. In particular, there were no varicose veins, telangiectases, or leg ulcers.

Based on the history and clinical findings, a diagnosis of stasis dermatitis was made. He was treated with betamethasone valerate ointment for nightly use. He was advised to keep his legs elevated when sitting, reading, watching television, or sleeping. He was also advised to start wearing 15 to 20 mm Hg below-knee compression socks every morning and to remove them just before bedtime.

Overview. Stasis dermatitis, also known as venous eczema, stasis eczema, venous stasis eczema, and gravitational dermatitis, is a dermatosis that occurs mainly on the lower legs and that is characterized by chronic dependent edema, hyperpigmentation, scaling, and induration with or without conspicuous varicose veins.^1-3

Prevalence. Stasis dermatitis typically affects individuals aged 50 years and older. It is estimated that the condition affects approximately 7% of individuals over 50 years of age and 20% of individuals over 70 years of age.^4,5 There is a slight female predominance.⁶

Etiopathogenesis. Stasis dermatitis is etiologically related to venous hypertension or chronic venous insufficiency.^7,8 Most cases are caused by incompetence of the intrinsic valves in either the superficial (long and short) saphenous veins or deep veins, and particularly incompetence of the communicating veins of the lower limb connecting the 2 venous systems.^6,9 Less commonly, venous hypertension results from obstruction to the venous flow (eg, DVT or thrombophlebitis), arteriovenous fistula, or failure of calf muscle pump that may occur with old age.^2,6,7,10 This accounts for the fact that stasis dermatitis can occur in the absence of varicose veins.

Predisposing factors for stasis dermatitis include obesity, multiple pregnancies, hypertension, heart failure, kidney failure, increased abdominal pressure, surgery (eg, vein stripping, total knee arthroplasty), traumatic injury to the leg, prolonged standing such as at work, and medications (eg, calcium channel blockers, β-blockers, minoxidil, clonidine, hydralazine, methyldopa, estrogen, nonsteroidal anti-inflammatory drugs).^2,3,11

The increased venous pressure leads to increased permeability of dermal capillaries, which allows fluid and macromolecules such as fibrinogen to leak out into interstitial spaces.¹² The accumulation of fluid in the interstitial spaces accounts for the edema. Polymerization of fibrinogen to fibrin results in the formation of a fibrin cuff around dermal capillaries, which serves as a barrier to oxygen diffusion, with resultant hypoxia and cell damage to the overlying skin and surrounding tissue.¹² Formation of fibrin cuffs and decreased cutaneous fibrinolytic activity lead to dermal fibrosis. The pigmentation seen in stasis dermatitis is due to deposition of hemosiderin in the skin and melanin pigment.^1,9 Dermal hemosiderin has a stimulatory effect on melanogenesis, which is associated with melanin incontinence.¹³

Histopathology. Histologic findings include hyperkeratosis, parakeratosis, acanthosis, and mild spongiosis in the epidermis; and lobular proliferation, dilatation, and distension of capillaries in the papillary dermis.^2,3,7 Other features include extravasated erythrocytes, hemosiderin-laden macrophages, perivascular lymphocytic infiltration, and dermal fibrosis.^2,3

Clinical manifestations. In the acute stage, patients often present with pruritus, edema, erythema, weeping, crusting, and scaling of the lower limbs.^5,12 In the chronic stage, hyperpigmentation, waxy or eczematous patches or plaques, hair loss, lichenification, induration, and thickened skin with a dimpled appearance may be seen.^2,3,5,12 Signs of venous hypertension or chronic venous insufficiency such as varicose veins, secondary lymphedema, and atrophie blanche can often be seen.²

Stasis dermatitis is usually bilateral but can be unilateral. The medial ankle is most frequently involved, and the lesion often extends up the leg and down to the foot.^1,2 Involvement of the upper limbs is unusual but may occur in patients who have an artificial arteriovenous fistula, for example, for hemodialysis.¹⁰

Diagnosis and differential diagnosis. The diagnosis is mainly clinical, based on the characteristic features. The diagnosis can be aided by dermoscopy. Dermoscopy typically shows glomerular vessels distributed in clusters or throughout the lesion.¹⁴ Patch testing can be performed for patients who experience a worsening of symptoms in spite of proper treatment to determine whether a contactant is present causing a secondary allergic contact dermatitis.² Color Doppler ultrasonography of the lower limbs should be considered if venous incompetence or DVT is suspected.²

The differential diagnosis includes atopic dermatitis, irritant contact dermatitis, allergic contact dermatitis, lichen simplex chronicus, hypertrophic lichen planus, asteatotic eczema, nummular eczema, psoriasis, tinea corporis, necrobiosis lipoidica, pretibial myxedema, Schamberg purpura, and cutaneous T-cell lymphoma.²

Complications and prognosis. Complications include lipodermatosclerosis, ulceration, contact sensitization, autosensitization (autoeczematization or id reaction), and superinfection (especially with Staphylococcus aureus or Streptococcus pyogenes).^2,11,12 Lipodermatosclerosis is a chronic form of panniculitis the chronic phase of which is characterized by hyperpigmented and indurated skin that constricts the ankle region, giving the legs an appearance of an inverted champagne bottle.² Stasis dermatitis has an adverse effect on the quality of life.³ Affected patients are at increased risk for squamous cell carcinoma and keratoacanthoma.^3,15

The prognosis is variable, depending on the underlying cause, but generally this is a chronic and difficult to manage condition.

Management. The underlying cause should be treated if possible. Should the patient have structural defects of the veins causing the stasis dermatitis, ligation or stripping of veins, endovenous laser ablation, radiofrequency ablation, and sclerotherapy can be used to treat the structural defects of the veins.¹² Offending medications should be discontinued. Patients who are obese may respond to decreased caloric intake, increased energy output, and behavioral modification. Patients should be advised to avoid clothing that restricts circulation or movement of the lower limbs.¹

General measures to reduce leg edema and venous hypertension include exercise, leg elevation, compression therapy (eg, compression socks, bandages, or stockings, pneumatic pumps), and proper skin care (use of bland emollients and nonsoap liquid cleansers).^2,12

High- or mid-potency topical corticosteroids are the mainstay of therapy for stasis dermatitis, particularly when pruritus is present.² Topical calcineurin inhibitors such as tacrolimus ointment and pimecrolimus cream are also good options. For recalcitrant stasis dermatitis, a short course of systemic corticosteroids can be considered.² Secondary bacterial infections, if present, should be treated with appropriate antibiotics.

Pigmentation due to stasis dermatitis may respond to noncoherent intense pulsed light.¹⁶ Studies have shown that oral ω-3 acid ethyl esters, as well as combination therapy with oral doxycycline and topical tacrolimus, are somewhat effective in controlling features of stasis dermatitis.^17,18 Further studies are needed to confirm these findings.

REFERENCES:

1. Englert K. Stasis dermatitis in the patient with CHF. Dermatol Nurs. 2003;​15(6):552.
2. Fransway AF. Stasis dermatitis. UpToDate. http://www.uptodate.com/contents/stasis-dermatitis. Updated December 8, 2016. Accessed June 23, 2017.
3. Weaver J, Billings SD. Initial presentation of stasis dermatitis mimicking solitary lesions: a previously unrecognized clinical scenario. J Am Acad Dermatol. 2009;61(6):1028-1032.
4. Beauregard S, Gilchrest BA. A survey of skin problems and skin care regimens in the elderly. Arch Dermatol. 1987;123(12):1638-1643.
5. Weiss SC, Nguyen J, Chon S, Kimball AB. A randomized controlled clinical trial assessing the effect of betamethasone valerate 0.12% foam on the short-term treatment of stasis dermatitis. J Drugs Dermatol. 2005;4(3):339-345.
6. Klassen W. Office management of stasis ulcer and stasis dermatitis. Can Fam Physician. 1983;29:279-283.
7. Dissemond J, Knab J, Lehnen M, Franckson T, Goos M. Successful treatment of stasis dermatitis with topical tacrolimus. Vasa. 2004;33(4):260-262.
8. Sippel K, Mayer D, Ballmer B, et al. Evidence that venous hypertension causes stasis dermatitis. Phlebology. 2011;26(8):361-365.
9. de Godoy JMP. Treatment of stasis dermatitis using aminaphtone: a case series. J Med Case Rep. 2010;4:295.
10. Deguchi E, Imafuku S, Nakayama J. Ulcerating stasis dermatitis of the forearm due to arteriovenous fistula: a case report and review of the published work. J Dermatol. 2010;37(6):550-553.
11. Gosnell AL, Nedorost ST. Stasis dermatitis as a complication of amlodipine therapy. J Drugs Dermatol. 2009;8(2):135-137.
12. Torrence BP, Hovanec R, Bartunek C, Brodell RT. Stasis dermatitis: practical pearls for the dermatologic nurse. Dermatol Nurs. 1993;5(3):186-191,208.
13. Rivera MR, Ishihara M, Mihara M. A case of non-selective phagocytosis of hemosiderin and melanin of dermal histiocytes in stasis dermatitis. Arch Dermatol Res. 2003;295(1):19-23.
14. Zaballos P, Salsench E, Puig S, Malvehy J. Dermoscopy of venous stasis dermatitis. Arch Dermatol. 2006;142(11):1526.
15. Harari Z, Zaidel L. Keratoacanthoma arising in stasis dermatitis. Dermatologica. 1983;167(6):322-325.
16. Pimentel CL, Rodriguez-Salido MJ. Pigmentation due to stasis dermatitis treated successfully with a noncoherent intense pulsed light source. Dermatol Surg. 2008;34(7):950-951.
17. Maroo N, Choudhury S, Sen S, Chatterjee S. Oral doxycycline with topical tacrolimus for treatment of stasis dermatitis due to chronic venous insufficiency: a pilot study. Indian J Pharmacol. 2012;44(1):111-113.
18. Nagai K, Matsumaru K, Hirai I, Takae Y, Andoh K. New therapy using omega-3-acid ethyl esters for decubitus ulcers and stasis dermatitis: a case report. Iran Red Crescent Med J. 2014;16(12):e19500.